Chooselife : In Edit
Life has exposed me to the tragic and devastating effects of Psychosis, both privately and professionally. During my time as a Support Worker, much first hand exposure to Psychosis has been part of the development path bestowed upon me.
These experiences lead to this topic and to seek White Paper evidence, which marries to the understanding which has been found. Which seems lacking by Healthcare Professionals generally, or ignored if understood.
Firstly, blood sugar, for several years, it seemed clear that severe Depression and Psychosis are Sugar fuelled, whether Hypoglycaemic driven depression, where the sugars are driven low for a prolonged period, or Hyperglycaemic where Sugars spike high, or worse spike and remain excessively high as seem in Psychosis.
The study below from 2002 is aptly linked as simply “Psychosis and Glucose” :
Assessment of independent effect of olanzapine and risperidone on risk of diabetes among patients with schizophrenia: population based nested case-control study
Glucose and psychosis
As Consultants in charge of Psychiatric Intensive care Units (PICU), we manage patients whose levels of arousal mean that they can not be managed on open acute psychiatric wards. All our patients have been compulsorily admitted under the terms of the Mental Health Act (England & Wales 1983).
We continuously monitor their physical condition, and this includes longitudinal monitoring of glucose levels. In addition, we monitor mental state using the Brief Psychiatric Rating Scale (BPRS), which gives an indication of the severity of the symptoms.
We report results in patients who have given their written informed consent to the publication of anonymised data, and who have agreed to form part of a study – approved by our local research ethics committee – of personal predictors on outcome in the PICU.
In forty-seven admissions to PICU, the glucose levels (mean 6.19 mmol/l SD 3.72)correlate with the BPRS on admission. If we exclude people with diagnosed non-insulin dependent diabetes, there is a direct correlation between BPRS at day 14 of the current admission and glucose levels during the first 7 days of the current admission (mean 5.13 mmol/l SD 0.93; p<_0.003 pearson=”pearson” correlation=”correlation” _0.477.=”_0.477.” p=”p”/>Twenty three admissions were treated with olanzapine (mean dose 32.85mg/day: BPRS 102.56 SD 29.13); twenty four were treated with risperidone (mean dose 7.58mg/day: BPRS 95.62 SD 14.29). At day 14, there were twenty one remaining (BPRS 72.38 SD 28.35) on olanzapine and twenty one on risperidone (BPRS 77.19 SD 20.09).
People with acute psychosis are highly aroused, and elevated glucose is not surprising. However, we suggest that control of glucose levels may be an important element of control of psychosis, and that elevated glucose levels – acute or chronic – may occur as part of the underlying psychosis, independently of the antipsychotic medication.
Psychotic patients often refuse to have blood tests. This can mean that, unless one is persistent in request for a sample (by a finger prick if necessary), one may miss hyperglycaemia.
Confronted with a psychotic patient who has abnormal glucose levels, psychiatrists may be tempted to modify or discontinue the antipsychotic drug for fear of precipitating a diabetic emergency.
We suggest that, on the contrary, adequate control of psychosis and disturbed behaviour with antipsychotic drugs may be necessary to prevent glucose spiralling out of control.
In addition, Convit et al (2003 PNAS 100: 2019-2022) have shown that reduced glucose tolerance may be associated with poor memory performance and hippocampal atrophy in elderly people who are not demented.
Hippocampal atrophy has been reported in psychotic disorders. Such studies do not, in the main, report the blood glucose, but it may be that, again as part of the underlying condition, disordered glucose may be pivotal.
Moreover, as hyperglycaemia is associated with both disturbed behaviour and microvascular disease, it is important to control for glucose in any assessment of the putative causal relationship of medication and microvascular (including cerebrovascular) disease.
The first client supported with Psychosis, would regularly seem (to me) to have incidents, after meals with high Potato content and/or Sugar, having unprompted outbreaks of screaming and attacking anybody near.
Now, reflections of clients supported, also leads me to consider the second link, that of constipation, though more broadly Bowel disturbance in general, much like sugar instability, appears to aggravate behaviours, in certain clients the mental and behavioural impact is devastating.
The Relation between Psychiatric Diagnoses and Constipation in Hospitalized Patients: A Cross-Sectional Study
Objective. Constipation is a prevalent problem in patients with psychiatric disorders; it reduces quality of life and may lead to severe complications.
The prevalence distribution of constipation across all psychiatric diagnoses in patients with severe mental illness (SMI) has hardly been studied. The aim of this study is to estimate the association between psychiatric disorders and constipation in SMI inpatients.
Methods. The strength of the association between constipation (based on use of laxatives) and DSM-IV psychiatric diagnosis was studied in a cross-sectional study with “adjustment disorders” as the reference group. The association was analyzed using logistic regression.
Results. Of the 4728 patients, 20.3% had constipation. In the stratum of patients older than 60 years, all psychiatric categories except for substance related disorders were significantly associated with a higher prevalence of constipation (odds ratios ranging from 3.38 to 6.52), whereas no significant associations were found in the stratum of patients between 18 and 60 years (odds ratios ranging from 1.00 to 2.03).
Conclusion. In the elderly, all measured psychiatric diagnoses are strongly associated with an increased prevalence of constipation. Physicians should be extra alert for constipation in SMI patients, independent of specific psychiatric diagnoses.
Chooselife : It is my empirical experience that Bowel Movement(s) appear to have a huge impact on averting or avoiding incidents of Psychosis.
Constipation and dyspepsia are disturbing gastrointestinal symptoms that are often ignored in research on physical comorbidities of schizophrenia. The aim was to assess dyspepsia and constipation in a sample of outpatients with schizophrenia spectrum psychoses.
A general practitioner performed a thorough physical health check for 275 outpatients and diagnosed constipation and dyspepsia. This study assessed the possible contribution of several sociodemographic, lifestyle, and clinical variables to constipation and dyspepsia using logistic regression analysis. This study also assessed whether these symptoms were associated with abnormal laboratory findings.
The prevalence of constipation was 31.3%, and of dyspepsia 23.6%. Paracetamol (OR =3.07, 95% CI =1.34-7.02) and clozapine use (OR =5.48, 95% CI =2.75-10.90), older age (OR =1.04, 95% CI =1.01-1.06), and living in sheltered housing (OR =2.49, 95% CI =1.16-5.33) were risk factors for constipation. For dyspepsia the risk factors were female sex (OR =2.10, 95% CI =1.15-3.83), non-steroidal anti-inflammatory drugs (OR =2.47, 95% CI =1.13-5.39), and diabetes medication (OR =2.42, 95% CI =1.12-5.25).
Patients with dyspepsia had lower haemoglobin and haematocrit and higher glucose values than those without dyspepsia.
Patients with constipation had lower thrombocyte values than patients without constipation.
However, these findings were explained by factors pre-disposing to constipation and dyspepsia.
Clozapine use markedly increases the risk of constipation and may lead to life-threatening complications. In addition, analgesics and diabetes medication were related to gastrointestinal symptoms. These medications and their association to gastrointestinal symptoms should be kept in mind when treating patients with schizophrenia.
Schizophrenia is a serious long-term psychotic disorder marked by positive and negative symptoms, severe behavioral problems and cognitive function deficits. The cause of this disorder is not completely clear, but is suggested to be multifactorial, involving both inherited and environmental factors. Since human brain regulates all behaviour, studies have focused on identifying changes in neurobiology and biochemistry of brain in schizophrenia. Brain is the most lipid rich organ (approximately 50% of brain dry weight). Total brain lipids is constituted of more than 60% of phospholipids, in which docosahexaenoic acid (DHA, 22:6n-3) is the most abundant (more than 40%) polyunsaturated fatty acid (PUFA) in brain membrane phospholipids. Results from numerous studies have shown significant decreases of PUFAs, in particular, DHA in peripheral blood (plasma and erythrocyte membranes) as well as brain of schizophrenia patients at different developmental phases of the disorder. PUFA deficiency has been associated to psychotic symptoms and cognitive deficits in schizophrenia. These findings have led to a number of clinical trials examining whether dietary omega-3 fatty acid supplementation could improve the course of illness in patients with schizophrenia. Results are inconsistent. Some report beneficial whereas others show not effective. The discrepancy can be attributed to the heterogeneity of patient population.
In this review, results from recent experimental and clinical studies, which focus on illustrating the role of PUFAs in the development of schizophrenia were examined. The rationale why omega-3 supplementation was beneficial on symptoms (presented by subscales of the positive and negative symptom scale (PANSS), and cognitive functions in certain patients but not others was reviewed. The potential mechanisms underlying the beneficial effects were discussed.
Omega-3 fatty acid supplementation reduced the conversion rate to psychosis and improved both positive and negative symptoms and global functions in adolescents at ultra-high risk for psychosis. Omega-3 fatty acid supplementation could also improve negative symptoms and global functions in the first-episode patients with schizophrenia, but improve mainly total or general PANSS subscales in chronic patients. Patients with low PUFA (particularly DHA) baseline in blood were more responsive to the omega-3 fatty acid intervention.
Omega-3 supplementation is more effective in reducing psychotic symptom severity in young adults or adolescents in the prodromal phase of schizophrenia who have low omega-3 baseline. Omega-3 supplementation was more effective in patients with low PUFA baseline. It suggests that patients with predefined lipid levels might benefit from lipid treatments, but more controlled clinical trials are warranted.
Omega-3 fatty acids in first-episode schizophrenia – a randomized controlled study of efficacy and relapse prevention (OFFER): rationale, design, and methods
Polyunsaturated fatty acid (PUFA) metabolism abnormalities have been long implicated in the etiology of schizophrenia. Although several randomized clinical trials have been carried out to assess the efficacy of omega-3 PUFA as add-on therapy in reducing psychopathology in populations of chronic patients with schizophrenia, only a few concern first-episode schizophrenia. The majority of these studies used a 12-week intervention based on ethyl-eicosapentaenoic acid (ethyl-EPA), however, with conflicting results. An intervention based on docosahexaenoic acid plus EPA has not been used in first-episode schizophrenia studies so far. No add-on supplementation studies have been carried out in medicated first-episode schizophrenia patients to assess the efficacy of omega-3 PUFA in preventing relapses.
A randomized placebo-controlled one-center trial will be used to compare the efficacy of 26-week intervention, composed of either 1320 mg/day of EPA and 880 mg/day of DHA, or olive oil placebo with regard to symptom severity and relapse rate in first-episode schizophrenia patients. Eighty-two patients (aged 16–35) will be recruited for the study. Eligible patients will be randomly allocated to one of two intervention arms: an active arm or a placebo arm (olive oil). The primary outcome measure of the clinical evaluation is schizophrenia symptom severity measured by the Positive and Negative Syndrome Scale (PANSS). Other outcomes include depressive symptoms, patient functioning and the level of insight. Correlates of change measured during the study will include structural brain changes, oxidative stress and defense, as well as neuroplasticity indicators. Metabolic syndrome components will also be assessed throughout the study.
By comparing 26-week administration of EPA + DHA or (placebo) olive oil as add-on therapy in reducing symptom severity and one-year relapse rate in patients with first episode schizophrenia, it is intended to provide new insights into the efficacy of omega-3 PUFA and correlates of change, and contribute to the improvement of mental health care for individuals suffering from schizophrenia.